Signs of Intracranial Hypertension, Hypermobility, and Craniocervical Obstructions in Patients With ME/CFS

sb4

Senior Member
Messages
1,522
Likes
2,628
Location
United Kingdom
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7485557/
Abstract
The pathophysiology of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is unknown. In this study, we test the hypothesis that hypermobility, signs of intracranial hypertension (IH), and craniocervical obstructions may be overrepresented in patients with ME/CFS and thereby explain many of the symptoms. Our study is a retrospective, cross-sectional study, performed at a specialist clinic for referred patients with severe ME/CFS as defined by the Canada Consensus Criteria. The first 272 patients with ME/CFS were invited to participate, and 229 who provided prompt informed consent were included. Hypermobility was assessed using the Beighton Score. IH was assessed indirectly by the quotient of the optic nerve sheet diameter (ONSD)/eyeball transverse diameter on both sides as measured on magnetic resonance imaging (MRI) of the brain. We also included assessment of cerebellar tonsil position in relation to the McRae line, indicating foramen magnum. Craniocervical obstructions were assessed on MRI of the cervical spine. Allodynia was assessed by quantitative sensory testing (QST) for pain in the 18 areas indicative of fibromyalgia syndrome (FMS). A total of 190 women, mean age 45 years, and 39 males, mean age 44 years, were included. Hypermobility was identified in 115 (50%) participants. MRI of the brain was performed on 205 participants of whom 112 (55%) had an increased ONSD and 171 (83%) had signs of possible IH, including 65 (32%) who had values indicating more severe states of IH. Cerebellar tonsils protruding under the McRae line into the foramen magnum were identified in 115 (56%) of the participants. MRI of the cervical spine was performed on 125 participants of whom 100 (80%) had craniocervical obstructions. Pain at harmless pressure, allodynia, was found in 96% of the participants, and FMS was present in 173 participants or 76%. Compared to a general population, we found a large overrepresentation of hypermobility, signs of IH, and craniocervical obstructions. Our hypothesis was strengthened for future studies on the possible relation between ME/CFS symptoms and hypermobility, IH, and craniocervical obstructions in a portion of patients with ME/CFS. If our findings are confirmed, new diagnostic and therapeutic approaches to this widespread neurological syndrome should be considered.
Just read the abstract. Seems like CFS patients has significantly more spine/brain issues that the general population. It seems they picked a random bunch of people with CFS but I am not sure, it says the study population was referred to them. I am trying to figure out if they where refereed because of suspected spinal issues or the referral was random.
 

Wishful

Senior Member
Messages
3,873
Likes
6,973
Location
Alberta
Very helpful. The intracranial hypertension might explain my double-vision. I'll have to ask my optometrist next time. Looking a bit deeper, I found that the double-vision from IH will affect one side more than the other, which is what I experience.

There's a drug to treat it. One possible side effect is sleepiness, which sounds quite delightful. :sleep: However, another description used the term 'drowsiness', which I consider to be more desire for sleep, but without actually making the person fall asleep easier, which is not at all helpful.
 
Messages
7,703
Likes
18,440
The intracranial hypertension might explain my double-vision. I'll have to ask my optometrist next time.
Sorry- I hate doctors.

Eye doctor- just said NO you don't have intracranial hypertension...when in fact I most likely do.

And my husband- I bring him to the appointment, to help me as I went thru this three years ago already- and that was a nothing result.

Doctors do nothing. Sorry but I am really angry about this. I don't get real mad any more very often as its a toxic emotion.

In my next life I will never obtain medical insurance. Thieves.
 

Pyrrhus

Senior Member
Messages
2,769
Likes
7,813
Location
U.S., Earth
Extract from the abstract:

Our study is a retrospective, cross-sectional study, performed at a specialist clinic for referred patients with severe ME/CFS as defined by the Canada Consensus Criteria. The first 272 patients with ME/CFS were invited to participate, and 229 who provided prompt informed consent were included. Hypermobility was assessed using the Beighton Score.
[...]
Hypermobility was identified in 115 (50%) participants.
[...]
[Fibromyalgia] was present in 173 participants or 76%.
[...]
Compared to a general population, we found a large overrepresentation of hypermobility, signs of [Intracranial Hypertension], and craniocervical obstructions.
 
Last edited:

Pyrrhus

Senior Member
Messages
2,769
Likes
7,813
Location
U.S., Earth
Related discussions:

ME/CFS Patients with Joint Hypermobility Show Larger Cerebral Blood Flow Reductions during Orthostatic Stress Testing... (van Campen et al., 2021)
https://forums.phoenixrising.me/thr...c-stress-testing-van-campen-et-al-2021.84635/

The Role of Cell Adhesion and Cytoskeleton Dynamics in the Pathogenesis of the Ehlers-Danlos Syndromes and Hypermobility Spectrum Disorders (Malek and Koester, 2021)
https://forums.phoenixrising.me/thr...s-and-hypermobility-spectrum-disorders.83712/

Neurological and spinal manifestations of the Ehlers–Danlos syndromes (Henderson et al., 2017)
https://forums.phoenixrising.me/thr...m-surrounding-peripheral-nerves-in-eds.77638/

Best model of hypermobility to explain the spectrum
https://forums.phoenixrising.me/threads/best-model-of-hypermobility-to-explain-the-spectrum.84012/

Hypermobile EDS and Hypermobility Spectrum Disorders what is the difference
https://forums.phoenixrising.me/thr...ctrum-disorders-what-is-the-difference.82929/

Hypermobility and treating a thumb that keeps falling out of place?
https://forums.phoenixrising.me/thr...eeps-falling-out-of-place.77533/#post-2231826

Has anyone noticed significant changes in their collagen? ( Vascular, Skin, Joints )
https://forums.phoenixrising.me/thr...in-their-collagen-vascular-skin-joints.80061/

RECURRENT MUSCULOSKELETAL INJURIES
https://forums.phoenixrising.me/threads/recurrent-musculoskeletal-injuries.77940/#post-2234644

Question about EDS
https://forums.phoenixrising.me/threads/question-about-eds.81988/

Other connective tissue illnesses (beside EDS) w CFS?
https://forums.phoenixrising.me/threads/other-connective-tissue-illnesses-beside-eds-w-cfs.78978/

Tests for connective tissue disorders?
https://forums.phoenixrising.me/threads/tests-for-connective-tissue-disorders.81742/#post-2303184

Does an EDS diagnosis actually help at all?
https://forums.phoenixrising.me/thr...osis-actually-help-at-all.78518/#post-2247545

Elastase 2 Inhibitors
https://forums.phoenixrising.me/threads/elastase-2-inhibitors.82035/#post-2320702

Have you ruled out Chiari or Craniocervical Instability (CCI) as a cause of your CFS
https://forums.phoenixrising.me/thr...instability-cci-as-a-cause-of-your-cfs.56908/
 
Last edited:

Pyrrhus

Senior Member
Messages
2,769
Likes
7,813
Location
U.S., Earth
On the topic of treatment of hypermobility:

There are different approaches to treating the poor collagen in hypermobility conditions. Some approaches target the mast cells that normally live in collagen-containing tissue, since these mast cells may degrade the surrounding collagen if they are degranulated on a frequent basis, releasing Matrix MetalloPeptidases (MMP) or elastases.

Another approach is to increase the dietary consumption of collagen ingredients, in order to allow your body to better maintain your collagen. Bone/cartilage broth is one way people consume the ingredients of collagen, since cartilage is made of collagen, and making a broth breaks down the cartilage into collagen.

I wonder whether one under-appreciated issue related to loss of cartilage in hypermobility conditions (and other conditions related to poor collagen) might be the role of glycine deficiency. Glycine is an amino acid that is essential for making or restoring cartilage. The average dietary intake of glycine is roughly 1.5-3 grams per day.[1] This is not enough for the body's needs, so the body makes its own glycine to make up for the inadequate dietary supply. However, the way that the body makes new glycine is tied to the folate cycle, which means that glycine production can be slowed down by anything that slows down the folate cycle, such as B12 deficiency or a reduced methylation capacity.[2]

One publication meticulously calculated the average body's glycine production and the average body's need for glycine. This paper found that the average body makes about 2.5 grams of glycine per day, but that the body needs a total of about 15 grams of glycine per day to maintain the amount of cartilage we had in early adulthood.[3] Although this is only one paper, their results may be supported by the in vitro observation that higher amounts of glycine continue to stimulate large increases in collagen synthesis, as if the cells know that the current collagen level must be inadequate.[4] (cartilage is made of collagen)

References
[1] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6627940/#idm139934315659552title
[2] https://pubmed.ncbi.nlm.nih.gov/19179765/
[3] https://pubmed.ncbi.nlm.nih.gov/20093739/
[4] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6153947/